Roles played by a subset of integrin signaling molecules in cadherin-based cell-cell adhesion

doi:10.1083/jcb.200312013

Published 19 July 2004. doi:10.1083/jcb.200312013
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 166, Number 2, 283-295

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Article

Roles played by a subset of integrin signaling molecules in cadherin-based cell–cell adhesion

Hajime Yano¹, Yuichi Mazaki¹, Kazuo Kurokawa², Steven K. Hanks³, Michiyuki Matsuda², and Hisataka Sabe¹^,4

¹ Department of Molecular Biology, Osaka Bioscience Institute, Osaka 565-0874, Japan
² Department of Tumor Virology, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan
³ Department of Cell Biology, Vanderbilt University School of Medicine, Nashville, TN 37232
⁴ Graduate School of Biostudies, Kyoto University, Kyoto 606-8502, Japan

Address correspondence to Hisataka Sabe, Dept. of Molecular Biology, Osaka Bioscience Institute, Osaka 565-0874, Japan. Tel.: (81) 6-6872-4814. Fax: (81) 6-6871-6686. email: sabe{at}obi.or.jp

Integrins can intercommunicate with cadherins. Here, we examinedtheir possible relationship by use of small interfering RNA–mediatedprotein knockdown in HeLa cells. We found that a subset of integrinsignaling molecules, namely Fak and paxillin, but not p130 Crk-associatedsubstrate or proline-rich tyrosine kinase 2, participate inprocesses regulating N-cadherin–based cell–celladhesion. Paxillin was found to be required primarily for therecruitment of Fak to robust focal adhesions. Our results suggestthat at least some signals involving Fak are linked to a mechanismdown-regulating Rac1 activity at the cell periphery, which appearsto be important for the formation of N-cadherin–basedadhesions in motile cells. Our analyses simultaneously exemplifiedthe essential role of Fak in the maintenance of cell–celladhesions in collective cell migration, a type of migrationoccurring in embryonic development and carcinoma invasion.

Key Words: Fak; integrin; N-cadherin; paxillin; siRNA

Abbreviations used in this paper: FA, focal adhesion; FAT, focaladhesion targeting; FRET, fluorescence resonance energy transfer;FRNK, Fak-related nonkinase; p130Cas, p130 Crk-associated substrate;Pyk2, proline-rich tyrosine kinase 2; siRNA, small interferingRNA.

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